RUSSIAN JOURNAL OF ELECTROCHEMISTRY
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2021
·Vol. 56
·期 12
·984-988
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IF 1.078
Zhixing Xiong,Ouyang Dilan,Zhang Wenbin
Abstract The use of 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) and 4-acetamido-TEMPO (ACT) for electrochemical oxidation of L-sodium lactate (SL) was comparatively investigated by cyclic voltammetry, and it was proved that ACT is more effective as a mediator in these electrocatalytic reactions. A comprehensive investigation of electrooxidation performance of ACT toward SL through investigating the effect of pH, concentration of SL, the sensitivity of SL using this electroanalytical method was calculated to be 2.78 μA cm –2 /mM, the catalytic rate constant was determined to be 51.7 L/(mol s) by using chronoamperometry.
研究领域:
电化学
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分析化学
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催化
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Advanced Science
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2025
·
IF 14.1
Jizhuo Li,Wenze Xun,Xijie Wang,Ruiguang Luo,Qifan Hu,Zhaocai Zhou,Jian Yuan,Yanan Wang,Xiaorui Wan,Tao Zhao,Tianyu Han,Jian-Bin Wang
Lactylation is a novel post-translational modification closely related to the glycolytic process, but the regulatory mechanisms between lactylation and glycolysis are far from being elucidated. Lactate dehydrogenase A (LDHA) catalyzes the formation of lactate, which provides the modifying group for protein lactylation. However, whether lactylation occurs on LDHA itself remains unknown. Here, it is found that lactylation promotes the enzymatic activity of LDHA in lung adenocarcinoma (LUAD), which in turn enhances the overall level of cellular lactylation through a positive feedback loop. Screening identified Lys81 and Lys318 as key LDHA lactylation sites, with alanyl-tRNA synthetase 1 (AARS1) serving as the mediating lactyltransferase. Mass spectrometry reveals that numerous proteins involved in DNA nonhomologous end junction (NHEJ), including FEN1, XRCC5, and XRCC6 might be regulated by lactylation. Delactylation of these proteins significantly hinders the formation of FEN1-RAD1-RAD9A-HUS1 complex, thereby leading to dysfunction of NHEJ and increasing the sensitivity of cancer cells to cisplatin. In summary, this work identifies LDHA lactylation as a critical mechanism for accelerating the progression of LUAD and reveals how this lactylation influenced cisplatin sensitivity of LUAD cells, which deepen the understanding of lactylation-mediated tumor progression and provide a potential new anticancer strategy.
研究领域:
癌症生物学
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分子生物学
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翻译后修饰
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代谢
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DNA修复
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肿瘤学
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
·
IF 4.7
Zhiqiang Wang,Man Li,Shuming Guo,Chen Deng,Beiyang Wang,Fang Gao,Junqiao Lv,Lin Sun
Ischemia and hypoxia near the injury site following spinal cord injury (SCI) lead to early lactate accumulation. Reactive astrocytes polarize and migrate to the lesion site, sealing it off and restricting immune cell infiltration. However, the specific mechanisms through which lactate influences astrocyte polarization remain poorly understood. In this study, we found that lactate can promote astrocyte proliferation, migration and differentiation into A2 after oxygen-glucose deprivation/reoxygenation (OGD/R). Inhibiting signal transducer and activator of transcription 3 (STAT3) nuclear transport reversed lactate-driven astrocyte polarization both in vivo and in vitro. Moreover, lactylome analysis identified nonhistone protein Ran as a target of lactylation at lysine 123 (K123). Ran silencing or mutation at K123 reversed the effects of lactate on STAT3 nuclear transport and astrocyte polarization. We also found that Ran lactylation is regulated by SIRT1. Taken together, our results show that lactate promotes astrocyte polarization via Ran lactylation-dependent regulation of STAT3 nuclear transport.
研究领域:
神经科学
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细胞生物学
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分子生物学
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代谢学
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WATER RESEARCH
·
2025
·
IF 12.4
Zhaozhao Gao,Xingjia Xiang,Meng Yan,Yongqi Liu,Yucheng Wu,Xin Song,Xiangui Lin,Frank E. Löffler,Jun Zeng
Microbial defluorination of per- and poly-fluoroalkyl substances (PFAS) likely involves cometabolic degradation. The isolation of pure cultures capable of this cometabolism would enhance our understanding of microbial defluorination mechanisms. Here, a novel isolate Sphingopyxis sp. strain NJF-3 was isolated and used to investigate the cometabolic defluorination of two poly-fluoroalkyl substances, 4,5,5-trifluoropent-4-enoic acid (TFEA) and 4,4,4-trifluoro-3-(trifluoromethyl)crotonic acid (SFCA). The isolate utilized 1-fluorodecane (FD) as the sole carbon source and released 873 ± 55 μM of inorganic fluoride (F⁻) from 1 mM FD within a 7-day incubation. The cometabolism of TFEA and SFCA by strain NJF-3 were significantly dependent on bacterial growth. Eleven cometabolic substrates were tested, revealing that 3,3-dimethylacrylic acid significantly stimulated TFEA defluorination, resulting in the removal of 27.3 ± 1.8 μM TFEA and the release of 71 ± 2.7 μM F⁻ over 28 days of incubation. Ammonium acetate promoted SFCA defluorination, leading to the degradation of 183 ± 17 μM SFCA and the release 736 ± 8.3 μM of F⁻ following 60 days of incubation. The integration of intermediate analysis with genomic data of strain NJF-3 revealed that the cometabolic biodefluorination proceeds via β -oxidation pathway, with hydroxylation-dehydration steps likely crucial for enzymatic C–F bond cleavage.
研究领域:
环境微生物学
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生物修复
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微生物代谢
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有机氟化学
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环境科学
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International Journal of Biological Sciences
·
2026
·Vol. 22
·期 4
·1775-1792
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IF 10
Shen Siman,Ying Chen,Fu Xinglin,Zeng Xiaobian,Guo Xiuli,Wu Han,Zhang Liangqing,Xu Li
Background: Persistently elevated glycolysis is increasingly recognized as a driving force in diabetic kidney disease (DKD). As a product of glycolysis, lactate can induce histone lactylation, an emerging epigenetic mechanism associated with post-transcriptional modification. However, the molecular mechanism and clinical impact of histone lactylation in DKD remain largely understood.Methods and Results: Spatial transcriptomics analysis revealed upregulation of glycolytic genes in tubular epithelial cells (TECs), thus leading to elevated levels of renal lactate accumulation. PKM2 deficiency lowered the lactate production during the fibrotic process and decreased histone lactylation. Mechanistically, ChIP-seq & RNA-seq results showed lactate promoted histone H4 lysine 12 lactylation (H4K12la), which in turn enhanced RUNX1 transcription. RUNX1 subsequently activated HK1 and SLC2A1, which accelerated glycolysis and renal fibrosis of DKD. Further, SIRT3 expression was significantly decreased in the renal tubular cells in DKD. Furthermore, insufficient SIRT3 is functionally promote renal fibrosis by directly deacetylating RUNX1 at H4K12, leading to attenuated glycolytic process, and subsequently robust glycolytic ability and increased production of lactate.Conclusion: Thus, the study links RUNX1-mediated glycolysis to SIRT3-mediated histonelactylation epigenetic reprogramming in promoting the fibrotic process, providing better understanding of epigenetic regulation of DKD pathogenesis, and new therapeutic strategy for DKD.
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Journal of Cleaner Production
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2026
·
IF 10
Bao Yu,Yuan Cheng,Tongbin Chen,Junxing Yang,Guodi Zheng
The pigsty is a major source of odor emissions, and effective on-site odor control is essential for improving the growth environment of pigs and reducing the burden on downstream deodorization systems. In this study, a simulated pigsty environment was used to systematically evaluate the deodorization efficacy of five organic acid salt solutions applied via surface spraying on pig manure. The objectives were to clarify their physicochemical solubilization effects, underlying microbial mechanisms and key functional taxa. Results showed that sodium lactate significantly outperformed the other organic acid salts, achieving an average reduction of 34.4 % ± 19.4 % in total odor activity over a 48-h cleaning period. This superior performance was primarily due to the effective inhibition of the key odorant p -cresol, with an average removal rate of 42.5 % ± 23.6 % and a peak removal rate of 76.8 % ± 1.2 % at 48 h. Analyses of the critical micelle concentration and Henry's law constant ruled out solubilization as the primary mechanism of p -cresol removal. Furthermore, changes in microbial biomass did not support the hypothesis that lactate deodorizes mainly via broad-spectrum bacterial inhibition. Instead, the primary mechanism involves enhanced microbial degradation of p-cresol. Notably, the biomass of the key bacterial genus Lentilactobacillus increased by 8.1–217.9-fold, promoting a microbial community that includes Faecalibaculum , Bifidobacterium , and Lachnospiraceae NK4A136_group . This community disrupts the stability of the odor-producing microbial symbiotic network through negative interactions. This study provides a new solution for controlling odor emissions from pig manure by identifying key microbial symbiotic mechanisms involved in odor production and inhibition.
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Signal Transduction and Targeted Therapy
·
2026
·Vol. 11
·期 1
·341
·
IF 81.2
Liu Shuai,Ma Yunfeng,Zeng Yujie,Lv Dekang,Hou Zhijie,Huang Junxiu,Gong Yaqi,Feng Ruijun,Wang Zihan,Sui Ran,Huang Dan,Wu Yameng,Chen Nuo,Yao Mingzhi,Shan Ying,Huang Yuan,Wang Yuesheng,Yan Jinsong,Peng Fei,Liu Quentin,Xu Jie
Activation of quiescent or extremely slow-cycling breast cancer stem-like cells (qsBCSCs) contributes to tumor progression, yet the regulatory mechanisms involved in triple-negative breast cancer (TNBC) remain elusive. We developed a dual-reporter system combining NANOG-EGFP and H2B-mCherry pulse-chase labeling to separately identify qsBCSCs and active BCSCs (aBCSCs) in vitro and in vivo. aBCSCs display significant enrichment of glycolysis and lactylation signatures, a finding corroborated by single-cell RNA sequencing (scRNA-seq) of TNBC patient samples. Glycolytic enzyme Enolase 1 (ENO1) expression is positively correlated with elevated histone H4 lysine 12 lactylation (H4K12la) in aBCSCs. Functional studies revealed a positive feedback circuit in which ENO1-increased lactate promotes H4K12la, which in turn activates ENO1 transcription. The ENO1-lactate-H4K12la axis enhances proliferating cell nuclear antigen ( PCNA ) transcription to activate qsBCSCs. Suppression of ENO1 or H4K12la prevents PCNA upregulation and qsBCSC activation. Importantly, PCNA knockdown alone blocks the activation of qsBCSCs induced by exogenous sodium L-lactate (NALA). In orthotopic breast cancer mouse models, both genetic depletion of ENO1 and pharmacological inhibition of lactate production attenuated tumor growth by blocking qsBCSC activation. Clinically, ENO1 expression was strongly correlated with PCNA expression, with high expression predicting poor OS, RFS, and DMFS. Our results establish the ENO1-H4K12la-PCNA axis as a key metabolic‒epigenetic driver of qsBCSC activation and a therapeutic target in TNBC.
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ONCOLOGY REPORTS
·
2026
·Vol. 56
·期 4
·1-12
·
IF 4.7
Jiawei Yu,Rui Pang,Bo Liu,Lili Chen,Jiewu Zhang
Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.
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Water Research X
·
2026
·
IF 7
Zhixiong Huang,Baobo Liu,Yi Wen,Jinpei Kuang,Wenle Peng,Jianwei Wang,Wenliang Lv,Michele Lancia,Lihong Yang
Acid Mine Drainage (AMD) poses global threats to ecosystems and has compelled the optimization of passive treatment systems via the understanding of internal hydrochemical and biological kinetics. This study systematically analyzed the performance of an integrated treatment scheme combining Anaerobic Limestone Drains (ALD) and Sulfate-Reducing Bacteria (SRB) through a multi-scale experimental and modeling approach. At the laboratory scale, the ALD reactor effectively neutralized highly acidic AMD (pH < 3.0) and favored the precipitation of Al- and Fe-hydroxides. However, the ALD exhibited lower efficiency for Zn 2+ and Mn 2+ removal, due to pH oscillations that altered the adsorption kinetics, as testified by reactive transport modeling in porous media. The encouraging ALD results prompted the construction of a pilot-scale ALD-SRB coupling system. Experimental results were complemented with a second numerical model to evaluate the sulfate removal performance. In the mature phase, observed and simulated results indicated a sulfate removal rate of 1.22 × 10 -4 mol m -3 s -1 ( R 2 > 0.92), which aligned with the stabilization of the Desulfovibrio -dominated syntrophic network. This integrated strategy confirmed the tight coupling between chemical and biological reaction kinetics, providing theoretical foundations and alternative approaches for optimizing upscaled passive AMD remediation.
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Stem Cell Reports
·
2026
·
IF 5.6
Zhishuai Zhang,Yuchan Mai,Jun Tang,Jiaying Ning,Yanjiao Qin,Jiaming Gu,Zhaozong Cao,Jian Liu,Tiancheng Zhou,Junwei Wang,Jeane L. Pan,Jiaheng Chen,Yanling Zhu,Guangjin Pan
Natural Killer (NK) cells generally exhibit dysfunction in tumor microenvironment (TME), significantly limiting their efficacy in antitumor therapy. Tumor cells display enhanced glycolysis, leading to lactic acid (LA) secretion and accumulation in the TME. Using human-induced pluripotent stem cell (hiPSC)-derived NK cells (iNKs) as a model, we demonstrate that LA induces substantial iNK dysfunction, including reduced survival, impaired IFN-γ secretion, and diminished tumor-killing capacity due to severely compromised mitochondrial function. To overcome LA-induced dysfunction, we knocked in an expression cassette for lactate dehydrogenase B (LDHB) into hiPSCs (LDHB-hiPSCs), enabling conversion of cellular lactate to pyruvate. iNKs derived from LDHB-hiPSCs (LDHB-iNKs) largely resisted LA-induced dysfunction, exhibiting enhanced cytotoxicity and improved survival in high-LA tumor tissues. Importantly, LDHB-iNKs show superior suppression of solid tumor formation in vivo . Our study provides a novel strategy to enhance NK cell therapy against solid tumors by reshaping the metabolic pathways.
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PROGRESS IN ORGANIC COATINGS
·
2026
·
IF 7.9
Xin Yu,Qinghe Gao,Guoxuan Li,Zhigang Lei,Chao Wang,Li Zhang,Huijuan Qian,Mingliang Zhu,Jin Huang,Conying Lu,Zhichao Zhang
Microbiologically influenced corrosion (MIC) induced by sulfate-reducing bacteria (SRB) severely threatens the service of metal materials, and traditional purely passive barrier coatings fail to withstand the continuous attack of biofilms. Herein, a ternary composite material (LDH-ZIF@CaO₂) composed of CoAl-LDH, ZIF-67, and CaO 2 was synthesized and incorporated into epoxy resin to construct an anti-corrosion coating that integrates active antibacterial and anti-corrosion properties. The study reveals that this composite possesses typical microenvironment responsiveness: in the acidic environment generated by microorganism metabolism, the Co ions released from the system can catalyze H₂O₂ (produced by CaO₂ hydrolysis) to undergo a Fenton-like reaction, generating highly oxidizing hydroxyl radicals (•OH) and singlet oxygen ( 1 O₂). This achieves highly efficient eradication of SRB and biofilm detachment. Electrochemical impedance spectroscopy (EIS) tests indicate that when the CaO₂ loading is 200 mg, the coating exhibits the optimal anti-corrosion performance, maintaining high compactness and high impedance characteristics even after 30 d of immersion, the impedance value is 10 8 Ω cm 2 , which is 2 orders of magnitude higher than that of epoxy resin systems. Furthermore, this paper thoroughly elucidates that the excessive addition of CaO₂ (400 mg) leads to filler agglomeration, internal gas pressure, and oxidative degradation of the resin matrix caused by excessive free radicals, which conversely accelerates coating failure. This study provides a new theoretical basis and strategy for designing microenvironment-responsive, anti-MIC coatings.
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INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
·
2026
·Vol. 58
·期 3
·1-13
·
IF 8.5
Mingkun Xu,Linhang Fu,Yulong Zhang,Xiuli Guo,Han Wu,Sijing Gao,Fei Xiao,Li Xu
International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.
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危险品化学品经营许可证（带存储）